Hepatic monooxygenase activity can be induced by many different environmental chemical contaminants, and measurement of this activity has been proposed as an environmental biomonitor. Using in situ caged catfish and largemouth bass, and collected wild killifish, environmental induction of hepatic CYP1A1 was investigated using catalytic enzyme assays, regiospecific metabolism, immunodetection, and nucleic acid hybridization. The purpose of these studies was to evaluate these techniques for detection of CYP1A1 induction as a potential environmental biomonitor of environmental chemical contamination. Exposure of catfish in cages to polyaromatic hydrocarbon‐ (PAH‐) and polychlorinated biphenyl‐ (PCB‐) contaminated river water for two, four, or six weeks resulted in fourfold increases in ethoxyresorufin‐O‐deethylase (EROD) activity and three‐ and fivefold increases in immunoreactive CYP1A1 protein and hybridizable CYP1A1 mRNA, respectively, when compared to laboratory water control values. Hybridizable CYP1A1 mRNA in caged largemouth bass increased 5.1‐fold at 1 d of exposure. Caged largemouth bass had 5‐, 1.4‐, and 0.8‐fold increases at 3 d and 6‐, 2.4‐, 0.4‐fold increases at 7 d of river water exposure in EROD, immunoreactive CYP1A1 protein, and CYP1A1 mRNA, respectively, when compared to laboratory water control values. Livers of killifish from a 2,3,7,8‐tetrachlorodibenzo‐p‐dioxin‐contaminated area had threefold higher EROD activity and similarly elevated immunoreactive CYP1A1 protein, a two‐ to fourfold increase in CYP1A1 mRNA, and a four‐ to eightfold increase in 6β‐hydroxyprogesterone activity, when compared to killifish livers sampled from a “clean” site. These results indicate that catalytic activity measurements, immunodetection, and nucleic acid hybridization may be used to detect environmental hepatic CYP1A1 induction in fish, and may be useful for the biomonitoring or screening of selected environments for chemical contamination.
